Primates and nonprimates differ significantly in their response to methanol administration. Only primates develop acidosis and ocular pathological changes following methanol administration. Therefore monkeys represent the only viable experimental animal model for studies concerned with the mechanism and treatment modalities of the human methanol poisoning syndrome. The biochemical basis for this difference between primates (e.g. monkeys) and nonprimates (e.g. rats) was found to be mainly due to the difference in their ability to oxidize formate (a methanol metabolite) to carbon dioxide. Compared to rats, monkeys oxidize formate at a much slower rate. Thus methanol administraition to monkeys results in the accumulation of formate which was found to be the major cause of acidosis and ocular pathological changes. Preliminary unpublished data indicated that young rats may oxidize formate at a much slower rate than do adult rats i.e. at a rate similar to that seen in monkeys. Therefore this proposal was designed to study the quantitative and qualitative aspects of formate metabolism in the young rat. This will be accomplished by constructing dose response curves (dose of injected formate vs rate of formate oxidation) for young rats of various ages (ranging between 2 to 12 weeks). This will identify which age group is potentially the most suitable one for further studies. The enzyme system(s) responsible for formate oxidation will then be identified by the use of specific enzyme inhibitors. On the basis of the obtained data, further studies are planned to evaluate the use of the young rat as an alternate experimental animal model in which the methanol poisoning syndrome can be adequately studied. This work may also contribute to our knowledge of the developmental aspects of the one carbon pool metabolism.